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タイトル
  • en BS69 cooperates with TRAF3 in the regulation of Epstein–Barr virus-derived LMP1/CTAR1-induced NF-κB activation
その他のタイトル
  • en Physical and functional interactions between BS69 and LMP1/CTAR1
作成者
    • en Ikeda, Osamu
    • en Miyasaka, Yuto
    • en Yoshida, Ryuji
    • en Mizushima, Akihiro
    • en Oritani, Kenji
    • en Kuroda, Makoto
    • en Yasui, Teruhito
    • en Fujimuro, Masahiro
    • en Matsuda, Tadashi
アクセス権 open access
主題
  • Other en BS69
  • Other en EBV
  • Other en LMP1
  • Other en TRAF3
  • Other en NF-κB
  • Other en transcription
  • NDC 464
内容注記
  • Abstract en Epstein-Barr virus latent membrane protein 1 (LMP1) activates NF-κB signaling pathways through two C-terminal regions, CTAR1 and CTAR2. Previous studies have demonstrated that BS69, a multidomain cellular protein, regulates LMP1/CTAR2-mediated NF-κB activation by interfering with the complex formation between TRADD and LMP1/CTAR2. Here, we found that BS69 directly interacted with the LMP1/CTAR1 domain and regulated LMP1/CTAR1-mediated NF-κB activation and subsequent IL-6 production. Regarding the mechanisms involved, we found that BS69 directly interacted with TRAF3, a negative regulator of NF-κB activation. Furthermore, small-interfering RNA-mediated knockdown experiments revealed that TRAF3 was involved in the BS69-mediated suppression of LMP1/CTAR1-induced NF-κB activation.
出版者 en Elsevier
日付
    Issued2010-03-05
言語
  • eng
資源タイプ journal article
出版タイプ AM
資源識別子 HDL http://hdl.handle.net/2115/42639
関連
  • isVersionOf DOI https://doi.org/10.1016/j.febslet.2010.01.060
  • PMID 20138174
収録誌情報
    • PISSN 0014-5793
    • NCID AA00642943
      • en FEBS Letters
      • 巻584 号5 開始ページ865 終了ページ872
ファイル
コンテンツ更新日時 2023-07-26